We propose to develop a systems description for vascular smooth muscle contractility in both the physiologically "normal" state, and during prolonged circulatory shock. This proposal will be accomplished by isolating the subcellular organelles of vascular smooth muscle responsible for the regulation of contractility. The following characteristics of the isolated organelles will be examined: 1) The isolation of aortic sarcoplasmic reticulum. The capacity and affinity of aortic sarcoplasmic reticulum to bind and store calcium will be examined. 2) The isolation of aortic mitochondria. The capacity and affinity to bind and store calcium will be examined. 3) The isolation of aortic myofibrils. The calcium and magnesium ATPase activity will be compared with known levels of calcium and magnesium necessary for tension development. Calcium binding will also be examined. 4) The isolation and identification of the sarcklemma. Calcium stimulated ATPase and adenyl cyclase activities of the sarcolemma will be examined. 5) The amount of sarcoplasmic reticulum, mitochondria, myofibrils, and sarcolemma per gram of aorta will be calculated. 6) Resultant data will be incorporated into a systems description of the regulation of intracellular calcium: the factor regulating contractility. 7) The influence of prolonged endotoxin and hemorrhagic shock on the systems description cf intracellular calcium regulation will be examined, the determine whether the detrimentalhemodynamic changes in shock can be explained by modified smooth muscle contractility.